T-cell lymphoma with rhabdomyolysis: case report and literature review.

Rhabdomyolysis refers to the destruction or disintegration of striated muscles. This syndrome is characterized by muscle breakdown and necrosis, resulting in the leakage of intracellular muscle constituents into the circulation and extracellular fluid. We report a rare case of rhabdomyolysis complicating multi-organ failure caused by T-cell lymphoma in a 32-year-old woman. The final diagnosis was rhabdomyolysis caused by peripheral T-cell lymphoma based on bone marrow aspirate and biopsy.

[Expression of syndecan-1 at different stages in the course of gastric carcinoma and its significance].

OBJECTIVE: To investigate the expression of syndecan-1 protein at different stages in the course of gastric carcinoma and its significance in carcinogenesis and metastasis. METHODS: There were 56 cases of chronic gastritis, 50 cases of chronic atrophic gastritis, 59 cases of intestinal metaplasia, 61 cases of displasia, and 112 cases of gastric carcinoma. Among the carcinoma cases, 55 were without and 57 with lymph node metastases. All paraffin-embedded tissue samples were assessed by immunohistochemistry. RESULTS: The syndecan-1 positive rate was 96.43% (54/56) in gastritis, 98.00% (49/50) in chronic atrophic gastritis, 100.00% (59/59) in intestinal metaplasia, 91.80% (56/61) in displasia, 45.45% (25/55) in gastric carcinoma without, and 24.56% (14/57) in gastric carcinoma with lymph node metastases. There was no significant difference among chronic gastritis, chronic atrophic gastritis and intestinal metaplasia (P > 0.05). There was a significant difference between displasia group and gastric carcinoma group (P <0.05), as well as between gastric carcinoma with and without lymph node metastases. There was a significant difference among well, moderately and poorly differentiated carcinoma groups. CONCLUSION: A decreasing expression of syedecan-1 in the development of gastric carcinoma is related with gastric carcinogenesis, and it may further promote metastasis of gastric carcinoma.

[Suppression of osteosarcoma in vitro by coexpression of antisense VEGF165 cDNA and thymidine kinase gene].

OBJECTIVE: To investigate the effect of VEGF expression in osteosarcoma cell line and the target killing effect of HSV1-TK/GCV system on transfected osteosarcoma cells under hypoxia conditions. METHODS: Eukaryotic expression plasmid with HRE promoter was constructed to express the antisense VEGF165 cDNA and Hygromycin phospho-transferase-thymidine kinase (HyTK) fusion gene. The recombinant vectors were then transfected into osteosarcoma cell line MG63 with lipofectin mediated gene transfer methods. PCR and RT-PCR were used to confirm the presence and expression of TK gene. The sensitivity of transfected cells to GCV and "bystander effect (BSE)" of HSV1-TK/GCV system under normoxia or hypoxia conditions were measured by MTT assay and mixed co-culture experiment. The expression of VEGF protein was detected by ELISA under hypoxia condition. Cell cycle phase distribution was determined by flow cytometry. In addition, electromicroscopy was used to document ultrastructural alterations. RESULTS: The eukaryotic expression vector pBI-HRE-AsVEGF165 -HyTK was constructed successfully. The transfected cell line MG63TV was established and confirmed by PCR and RT-PCR of the presence of transgene and its mRNA expression. GCV was toxic to transfected cells in a concentration-dependent manner. The sensitivity to GCV toxicity was 100 times higher under hypoxia condition than that under normoxic condition. The mixed culture experiments showed that the "bystander effect" was enhanced significantly under hypoxia condition. VEGF expression of transgene cells under hypoxia condition decreased 50% compared to that of normal condition. Under hypoxia and GCV, DNA synthesis of MG63TV cells was inhibited along with an increase of cells at G0 approximately G1 phase, apoptosis and necrosis. CONCLUSIONS: Antisense VEGF expression driven by HRE promoter in combination with hypoxia can provide a target inhibition of VEGF expression in human osteosarcoma cells, with an enhanced selective killing effect and BSE of the HSV-TK/GCV system. The double-gene co-expression system in study provides experimental basis for therapy against osteosarcoma by a synchronous antiangiogenic and suicide gene approach.

[Expression of microvessel density in multistep tissues of gastric carcinoma and significance thereof].

OBJECTIVE: To investigate the expression of microvessel density (MVD) in multistep tissue of gastric carcinoma and CD34 in the multistep tissue of gastric carcinogens. METHODS: 277 specimens of gastric diseases, 56 specimens of chronic gastritis, 50 specimens of chronic atrophic gastritis, 59 specimens of intestinal metaplasia, 61 specimens of dysplasia, 57 specimens of gastric carcinoma with lymph node metastases, and 55 specimens of gastric carcinoma without lymph node metastases, obtained from pathological department, Sun Yat-sen university, underwent pathological examination and immunohistochemistry to detect the expression of CD34 antigen that is expressed only in the endothelial cells in tumor. RESULTS: The mean MVD was 13 +/- 10 in the specimens of chronic gastritis, 11 +/- 7 in the chronic atrophic gastritis group, 13 +/- 9 in the intestinal metaplasia group, 17 +/- 10 in the dysplasia group, 27 +/- 11 in the gastric carcinoma without lymph node metastases group, and 28 +/- 10 in the gastric carcinoma with lymph node metastases group. There were not significant differences in MVD among the chronic gastritis group, chronic atrophic gastritis group, and intestinal metaplasia group (all P > 0.05), there was a significant difference in MVD between the chronic gastritis group and dysplasia group (P < 0.05). In the specimens of gastric carcinoma, there were no significant difference in MVD between those with and without lymph node metastases (P > 0.05), and between those of high and low differentiation degrees (both P < 0.05). CONCLUSION: The increase of expression of CD34 in the multistage tissues of gastric carcinoma is associated with the genesis of gastric cancer, and not be related to the gastric carcinoma metastases.

[The role of CD44 in the proliferation, adhesiveness and invasiveness of osteosarcoma cell lines].

OBJECTIVE: To study the influence of CD44 a cell-matrix adhesion molecule on the proliferation, adhesiveness and invasiveness of osteosarcoma cell lines, in order to investigate the growth and invasion mechanism of osteosarcoma. METHODS: Three osteosarcoma cell lines MG-63, HOS and U2-OS were routinely cultured. Flow cytometry and Western blot analysis were used for detecting the positive rates and relative amount of CD44 protein in the three cell lines. RT-PCR method was also used to compare the differences in the expression of CD44 mRNA among the 3 cell lines. Then, MTT method, adhesion detection, and Microcon-migration assay were used to detect the changes of the cells' proliferation rate, adhesive and invasive abilities after blocking the role of CD44 by using a special neutralizing antibody. RESULTS: The results of flow cytometry showed that the percentage of CD44 positive cells were both over 99% in HOS and U2-OS, while that in MG-63 was only (2.10 +/- 0.46)%. The average fluorescence density of CD44 in HOS was significantly higher than in U2-OS. Western blot also showed that the relative content of CD44 protein in HOS was notably higher than that in U2-OS, while CD44 was negatively expressed in MG-63. The expression of CD44 mRNA was significantly lower in MG-63 than in both HOS and U2-OS, which were consistent with the expression of CD44 protein. The proliferation rates and adhesive abilities of MG-63 and HOS have no significant difference, but both were significantly higher than that of U2-OS. The invasive abilities of HOS was dramatically higher than MG-63 and U2-OS. After the role of CD44 was blocked by anti-CD44 neutralizing antibody, the proliferation rates of the 3 cell lines did not change significantly. While the HOS and MG-63 adhesion indices decreased dramatically (P < 0.05), the invasive abilities of HOS and U2-OS also decreased notably (P < 0.01). CONCLUSIONS: CD44 could promote the adhesiveness and invasiveness of osteosarcoma cell line HOS. CD44 may take part in promoting the process of U2-OS invasion and the adhesion of MG-63. On the other hand, CD44 could not affect the osteosarcoma cell proliferation rates.

[Targeted inhibition of vascular endothelial growth factor (VEGF) expression in human osteosarcoma cell line by antisense VEGF165 cDNA promoted by hypoxia reaction element].

OBJECTIVE: Utilizing the hypoxia inducible factor 1/hypoxia reaction element (HIF-1/ HRE) gene regulation system to construct antisense vascular endothelial growth factor (VEGF165) cDNA eukaryotic expression vector promoted by HRE, and investigate its targeted inhibiting VEGF expression of osteosarcoma cells in hypoxia environment. METHODS: Eukaryotic expression plasmid with HRE promoter was constructed containing luciferase reporter gene and antisense VEGF165 cDNA by using PCR and recombinant DNA techniques. The recombinant vectors were transfected into osteosarcoma cells with lipofectin method. Hypoxia-inducible reporter gene expression was determined by liquid scintillation analyzer and the expression of VEGF protein was detected by ELISA method. RESULTS: The eukaryotic expression plasmid containing antisense VEGF165 and luciferase promoted by HRE was constructed successfully. After being transferred into MG63 cells, luciferase expression was increased 3.5 x 10(2) times and VEGF protein expression decreased 45% under hypoxia condition. CONCLUSION: Antisense VEGF165 cDNA expression, efficiently realized by HRE promoter under hypoxia condition, provides an experimental basis for targeted antiangiogenesis of tumors.

Expression of CD44v3, erythropoietin and VEGF-C in gastric adenocarcinomas: correlations with clinicopathological features.

AIMS: To investigate the expression of CD44v3 and vascular endothelial growth factor C (VEGF-C) in gastric adenocarcinoma and the correlation with erythropoietin (EPO) and clinicopathological features. METHODS: The expression of CD44v3, VEGF-C and EPO was evaluated by immunohistochemical staining in 169 gastric adenocarcinomas. The correlations between these parameters and patients' clinicopathological features were analyzed statistically. RESULTS: CD44v3 and VEGF-C were positive in 50 (29.6%) and 82 (48.5%) patients, respectively. High CD44v3 expression was associated with poor cellular differentiation, extensive lymph node metastasis and advanced stage of gastric adenocarcinoma (P <0.05). High VEGF-C expression was significantly correlated with Lauren type, extensive lymph node metastasis and advanced stage of gastric adenocarcinoma (P <0.05). Univariate analysis of survival demonstrated that patients with a strong CD44v3 immunoreaction had a significantly worse overall survival compared with patients showing a weak CD44v3 immunoreaction (log-rank test: P = 0.0449). The mean survival time of patients with low CD44v3 expression was 30.6 months, which was much longer than the 21.6 months in patients with high expression. In addition, a strong association between immunohistochemical expression of CD44v3 and EPO was noted. CONCLUSION: Increased expression of CD44v3 and VEGF-C may play a significant role in the carcinogenesis and progression of gastric adenocarcinoma. High CD44v3 expression may be a predictor of poor prognosis in gastric adenocarcinoma patients. We infer that some mechanisms may exist in regulating the expression of CD44v3 and EPO.

T-cell lymphoma with rhabdomyolysis: case report and literature review

Rhabdomyolysis refers to the destruction or disintegration of striated muscles. This syndrome is characterized by muscle breakdown and necrosis, resulting in the leakage of intracellular muscle constituents into the circulation and extracellular fluid. We report a rare case of rhabdomyolysis complicating multi-organ failure caused by T-cell lymphoma in a 32-year-old woman. The final diagnosis was rhabdomyolysis caused by peripheral T-cell lymphoma based on bone marrow aspirate and biopsy.

IMP3 is a novel biomarker to predict metastasis and prognosis of gastric adenocarcinoma: a retrospective study.

BACKGROUND: Insulin-like growth factor-II mRNA-binding protein 3 (IMP3) is a newly identified mRNA-binding protein that is involved in embryogenesis and carcinogenesis of some malignant tumors. The aim of this study was to detect the expression of IMP3 protein in gastric adenocarcinoma (GAC) and the correlation with clinicopathological features. METHODS: IMP3 protein in 92 samples of GAC was evaluated by immunohistochemical method. The Mann-Whitney U test and Kruskal-Wallis H test were used to compare IMP3 expression and clinicopathological parameters. Kaplan-Meier survival curve, log-rank test and Cox-regression model were used to evaluate the correlation of IMP3 protein expression to the prognosis of patients. RESULTS: Out of 92 cases of adjacent normal mucosa (ANM), 10 with dysplasia demonstrated weak expression of IMP3 and 82 without dysplasia showed negative expression. Out of 92 cases of GAC, positive immunohistochemical stain for IMP3 was identified in 75 (82%) cases. A comparison of IMP3 expression in GAC and ANM showed stronger immunohistochemical reactivity in GAC (P < 0.05). High expression of IMP3 was found to be associated with lymphoid metastasis, high Ki-67 labelling index, and patient poor outcome (P < 0.05). There was a significant TNM stage difference between GAC with and without IMP3 expression (P < 0.05). Tumors with higher stage showed higher level of IMP3 expression. In multivariate analysis, IMP3 emerged as an independent predictor of survival. CONCLUSIONS: Increase of IMP3 expression suggests that IMP3 may play an importent role in the carcinogenesis and tumor metastasis in GAC. It could be regarded as a novel proliferation and prognostic indicator for patients with GAC.

[Expressions of CD44s, MMP-9, and Ki-67: possible association with invasion, metastasis, and recurrence of osteosarcoma].

BACKGROUND & OBJECTIVE: Recent research had showed that tumor cell adhesion molecular CD44 and matrix metalloproteinases (MMP) were expressed strongly in many tumors, and was associated closely with invasion and metastasis of the tumors. Ki-67 was one of the proliferative markers, which indicated the growth rate of tumor cells. However, the relationship among these markers and the invasion, metastasis, and recurrence of osteosarcoma was unclear yet. In this research the authors studied the expression of standard-type CD44(CD44s), MMP-9, and Ki-67 in osteosarcoma, and their relation to the invasion, metastasis, and recurrence of the tumor. METHODS: Immunohistochemistry staining(SP method) was used to detect CD44s, MMP-9, and Ki-67 in cases of osteosarcoma. Bone benign disease or normal connective tissue were used as the control. The results were treated with semi-quantitative method and analyzed by using non-parameter rank sum test. RESULTS: The positive rates of CD44s, MMP-9, and Ki-67 in osteosarcoma were 71.0%, 75.8%, and 35.5%, respectively, which were significantly higher than that in control tissue. The positive rate of Ki-67 in recurrent osteosarcoma was 81.8%, which was significantly higher than that in primary tumor. CD44s and Ki-67 positive rates were 88.9% and 66.7% respectively in osteosarcoma with lung metastasis, which were both significantly higher than that in osteosarcoma without lung metastasis. In poorly differentiated osteosarcoma positive rates of CD44s and MMP-9 were 76.3% and 79.7%, respectively, which were significantly higher than that in well differentiated tumor. Spearman correlation analysis proved that the expression of CD44s, MMP-9, and Ki-67 had significant relation to another. CONCLUSIONS: Increase of CD44s, MMP-9, and Ki-67 were involved in the growth and local invasion of osteosarcoma. The recurrence of osteosarcoma was associated with the proliferative rate of tumor cells. Whether there were early lung metastasis or not was affected by the amount of CD44s and the proliferative rate of the tumor cell. The poorer differentiation of osteosarcoma cells, the higher level of CD44s and MMP-9.